摘要
目的 研究A3 活性部位抑制子宫平滑肌收缩的机制。方法 采用离体大鼠子宫肌张力记录法和Westernblot方法。结果 A3 活性部位可明显拮抗前列腺素F2α (PGF2α)诱发的离体子宫收缩增强作用 ,但此作用不被PGF2α逆转 ;在经吲哚美辛处理的标本上 ,再给A3 活性部位 ,其抑制离体子宫作用明显增强。A3 活性部位 ( 4 0和 80mg/L)抑制正常和PGF2α增高的大鼠子宫平滑肌组织 p4 2 / 4 4丝裂原激活蛋白激酶 (p4 2 / 4 4MAPK)磷酸化水平和间隙连接蛋白 4 3(Cx4 3蛋白 )表达水平。结论 A3 活性部位抑制子宫收缩作用机制与其抑制PGF2α下游 p4 2 / 4 4MAPK Cx4
Objective To study the mechanism of inhibitory effect of A 3 active component (active site, A 3) from Angelica naphtha on myometrium contraction. Methods Recording of the uteruses smooth muscles tensity and Western blot were used.Results A 3 (10-80 g/kg) could dose dependently antagonize the effect of prostaglandin F 2α (PGF 2α ) on rat myometrium contraction. But this effect could not be reversed by PGF 2α . Moreover, the inhibitory effect of A 3 was potentiated by Indomethacin. A 3 (40, 80 mg/L) inhibited basal and PGF 2α stimulated p42/44 mitogen activated protein kinase (p42/44 MAPK) activity and connexin 43 (Cx43) protein expression. Conclusion The mechanism of the inhibitory effect of A 3 on myometrium contraction may be related with the inhibition of the down stream signaling of PGF 2α , especially with mitogen actived protein kinase (MAPK) connexin 43 pathway.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2003年第5期471-473,477,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目 (No 30 1710 95 )
